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Medical or surgical treatment for patients with carotid stenosis?
Vol. 65, Suppl. 1
ABSTRACTS OF 12TH INTNAT’L CONGRESS
s17
s30 MEDICAL OR SURGICAL TREATMENT FOR PATIENTS WITH CAROTID STENOSIS? H.J.M. Bamett Robarts Research Institute, London, Ontario, CDN The clinical trials to determine strategies which will prevent strolls have not baen daslgnad to examme best medical therapy versus placebo ln Patients spedfically afflicted with carotid artery disease. Nevertheless it seems reasonable to take it for granted that patients with TIA and minor stroke arising from carotid lesions should be treated by risk factor management and platelet-inhibiting drugs. The latter have now baen narrowed down to aspirin and ticlopidine. There remains a controversy over the optimum dose of aspirin. Surgical therapy has been evaluated in symptomatic and asymptomatic patients with carotid artery disease, and for patients submitted to superficial temporal to middle cerebral artery anastomosis and to carotid endarterectomy. There is no evidence that bypassing occluded or inaccessibly stenosed carotid arteries reduces the risk of stroke nor improves the functional status of these patients. The North American and the European trials of carotid endartemctomy have found unequivocal benefit for the procedure in Patients with tight stenosis (> 70% by strict angiographic measurements). A declining benefit from surgery from the 9th to the 7th declle of Percentage stenosis yielded a difference at 2 years of stroke-free survival in the medical and surgical groups of 27%, 19% and 12% respeaively. No data am available from these ongoing trials which declare benefit yet for Patients with less than 70% stenosis. Secondary studies from NASCET have determined that the presence of radiologically visualized ulceration, the finding of asymptomatic CT brain infarction in those presenting with TIA, and the occurrence of hemisphere as compared with retinal events adds significantly to the gravity of the prognosis.
S31 REGULATION OF THE RESPONSE TO THROMBOXANE A2 G.A. Fitzgerald Center for Cardiovascular Science, Mater Hospital, University College, Dublin, IR Thromboxane A2 plays a key role in amplification of the response to a variety of platelet agonists; inhibition of its synthesis and/or action has been shown to reduce cardiovascular morbidity. It is thought to mediate its effects on platelets and vascular tissue via heptahelical receptors coupled to phospholipase activation via G proteins, including those of the Gq family and a novel 60kDa protein, Ge.Pharmacological experiments suggest the existence of two forms of the receptor in human platelets, mediating shape change and aggregation. The response to thromboxane A2 is regulated at multiple levels, including expression and mechanism based inactivation of its synthetic enzymes, receptor-G protein uncoupling with subsequent receptor internalization and thromboxane mediated endothelial release of the counterregulatory eicosanoid, prostacyclin. Finally, the cellular response to Gs-linked activation of adenylate cyclase is enhanced coincident with TX receptor desensitization in human platelets.
ABSTRACTS OF 12TH INTNAT’L CONGRESS
s17
s30 MEDICAL OR SURGICAL TREATMENT FOR PATIENTS WITH CAROTID STENOSIS? H.J.M. Bamett Robarts Research Institute, London, Ontario, CDN The clinical trials to determine strategies which will prevent strolls have not baen daslgnad to examme best medical therapy versus placebo ln Patients spedfically afflicted with carotid artery disease. Nevertheless it seems reasonable to take it for granted that patients with TIA and minor stroke arising from carotid lesions should be treated by risk factor management and platelet-inhibiting drugs. The latter have now baen narrowed down to aspirin and ticlopidine. There remains a controversy over the optimum dose of aspirin. Surgical therapy has been evaluated in symptomatic and asymptomatic patients with carotid artery disease, and for patients submitted to superficial temporal to middle cerebral artery anastomosis and to carotid endarterectomy. There is no evidence that bypassing occluded or inaccessibly stenosed carotid arteries reduces the risk of stroke nor improves the functional status of these patients. The North American and the European trials of carotid endartemctomy have found unequivocal benefit for the procedure in Patients with tight stenosis (> 70% by strict angiographic measurements). A declining benefit from surgery from the 9th to the 7th declle of Percentage stenosis yielded a difference at 2 years of stroke-free survival in the medical and surgical groups of 27%, 19% and 12% respeaively. No data am available from these ongoing trials which declare benefit yet for Patients with less than 70% stenosis. Secondary studies from NASCET have determined that the presence of radiologically visualized ulceration, the finding of asymptomatic CT brain infarction in those presenting with TIA, and the occurrence of hemisphere as compared with retinal events adds significantly to the gravity of the prognosis.
S31 REGULATION OF THE RESPONSE TO THROMBOXANE A2 G.A. Fitzgerald Center for Cardiovascular Science, Mater Hospital, University College, Dublin, IR Thromboxane A2 plays a key role in amplification of the response to a variety of platelet agonists; inhibition of its synthesis and/or action has been shown to reduce cardiovascular morbidity. It is thought to mediate its effects on platelets and vascular tissue via heptahelical receptors coupled to phospholipase activation via G proteins, including those of the Gq family and a novel 60kDa protein, Ge.Pharmacological experiments suggest the existence of two forms of the receptor in human platelets, mediating shape change and aggregation. The response to thromboxane A2 is regulated at multiple levels, including expression and mechanism based inactivation of its synthetic enzymes, receptor-G protein uncoupling with subsequent receptor internalization and thromboxane mediated endothelial release of the counterregulatory eicosanoid, prostacyclin. Finally, the cellular response to Gs-linked activation of adenylate cyclase is enhanced coincident with TX receptor desensitization in human platelets.